ライフサイエンスコーパス: atherosclerotic lesion

1 , progression, and subsequent rupture of the atherosclerotic lesion.

2 cessary processes for the progression of the atherosclerotic lesion.

3 ce inhibited monocyte recruitment to nascent atherosclerotic lesions.

4 ct >80% of SMC-derived cells within advanced atherosclerotic lesions.

5 ion of vascular cell migration and matrix in atherosclerotic lesions.

6 studies of HDL-like particles recovered from atherosclerotic lesions.

7 duced the development of both early and late atherosclerotic lesions.

8 quantification of VCAM-1 expression in mouse atherosclerotic lesions.

9 ndothelial activation and the development of atherosclerotic lesions.

10 ival, as well as differentiation in advanced atherosclerotic lesions.

11 g emerges as a new tool for the detection of atherosclerotic lesions.

12 ) have long been recognized as a hallmark of atherosclerotic lesions.

13 percholesterolemia and a marked elevation in atherosclerotic lesions.

14 on and make up a major component of advanced atherosclerotic lesions.

15 imaging agent for the detection of inflamed atherosclerotic lesions.

16 the in vivo imaging of VCAM-1 expression in atherosclerotic lesions.

17 ue to inconsistent detection of the virus in atherosclerotic lesions.

18 n in the lymphoid system and the presence in atherosclerotic lesions.

19 hancing recruitment of Ly6c(hi) monocytes to atherosclerotic lesions.

20 ration of both effector T cells and Tregs in atherosclerotic lesions.

21 ls, necrotic cores, and interleukin 1beta in atherosclerotic lesions.

22 demia to cause topographical distribution of atherosclerotic lesions.

23 n apoptotic cells, inflammatory tissues, and atherosclerotic lesions.

24 educe macrophage cholesterol accumulation in atherosclerotic lesions.

25 m the arterial lumen and the adventitia into atherosclerotic lesions.

26 nd are at great risk to develop obstructive, atherosclerotic lesions.

27 is a major contributor to the instability of atherosclerotic lesions.

28 in SPC migration and their recruitment into atherosclerotic lesions.

29 rculating inflammatory cells that infiltrate atherosclerotic lesions.

30 d neutrophilia and how neutrophils may enter atherosclerotic lesions.

31 LDL, C3, C3a, and TLR4 during development of atherosclerotic lesions.

32 hat pDCs can be detected in murine and human atherosclerotic lesions.

33 ction may be important in the development of atherosclerotic lesions.

34 and platelet activation in the formation of atherosclerotic lesions.

35 lls (SMCs), and endothelial cells from mouse atherosclerotic lesions.

36 oth muscle actin-positive SMC areas in their atherosclerotic lesions.

37 inflammatory M1 macrophages into developing atherosclerotic lesions.

38 DL) in endothelial cells, is up-regulated in atherosclerotic lesions.

39 IRF5 affects the formation and phenotype of atherosclerotic lesions.

40 CAM1 nanobodies for noninvasive detection of atherosclerotic lesions.

41 s a relevant target for molecular imaging of atherosclerotic lesions.

42 E -/- mice, hArgII mice had increased aortic atherosclerotic lesions.

43 accumulation of oxidized lipoproteins within atherosclerotic lesions.

44 , neutrophilia, and monocyte accumulation in atherosclerotic lesions.

45 plasma cholesterol and TG levels and reduced atherosclerotic lesions.

46 ay allow for molecular imaging of vulnerable atherosclerotic lesions.

47 ulation is a key characteristic of advancing atherosclerotic lesions.

48 que inflammation and progression to advanced atherosclerotic lesions.

49 and macrophage-derived foam cells and cause atherosclerotic lesions.

50 f bifurcated vessels that are susceptible to atherosclerotic lesions.

51 ) mice have a significant increase of aortic atherosclerotic lesions.

52 etion in myeloid cells increased the size of atherosclerotic lesions.

53 lipid-laden macrophages that infiltrate the atherosclerotic lesions.

54 lerosis by enhancing monocyte recruitment to atherosclerotic lesions.

55 -specific ABCG1 deficiency protected against atherosclerotic lesions.

56 ced endothelial inflammation and the size of atherosclerotic lesions.

57 e circulation and alter cellular behavior in atherosclerotic lesions.

58 notypes and the consequential development of atherosclerotic lesions.

59 racy of measurements and characterization of atherosclerotic lesions.

60 es of stability, and monocyte recruitment to atherosclerotic lesions.

61 rosclerosis, to resolution and regression of atherosclerotic lesions.

62 kine production, and increased cell death in atherosclerotic lesions.

63 In Apoe(-/-) mice with mature atherosclerotic lesions (5 months of high fat diet), we

64 less hepatic lipid accumulation and smaller atherosclerotic lesions (60% smaller in Ldlr(-/-);Gsk3a(

65 Although not detected in atherosclerotic lesions, Abcg4 was highly expressed in b

66 e marrow cells exhibited significantly fewer atherosclerotic lesions after high-fat and high-choleste

67 RI showed an increased uptake of NP-HDL into atherosclerotic lesions after intraperitoneal injection,

68 A, inflammasome activation, and apoptosis in atherosclerotic lesions and also higher serum IL-1beta a

69 t-like structures have also been detected in atherosclerotic lesions and arterial thrombi in humans a

70 ice, Nef significantly increased the size of atherosclerotic lesions and caused vessel remodeling.

71 Because eRNA is associated with atherosclerotic lesions and contributes to inflammation-

72 markedly enhanced in patients with advanced atherosclerotic lesions and correlates with disease seve

73 ortant research tool for targeted imaging of atherosclerotic lesions and has the potential for fast c

74 phospho-IRE1, and GRP78 in macrophage-dense atherosclerotic lesions and in peritoneal macrophages.

75 one marrow into Ldlr(-/-) mice led to larger atherosclerotic lesions and increased IL-1beta productio

76 Furthermore, DMAG significantly reduced atherosclerotic lesions and induced a more stable plaque

77 d to alteration of monocyte recruitment into atherosclerotic lesions and inhibited toll-like receptor

78 if ligand 16 (CXCL16) is highly expressed in atherosclerotic lesions and is a potential pathogenic me

79 C3 is expressed in human atherosclerotic lesions and is involved in atherogenesis

80 AMPKalpha1(-/-) mice showed reduced sizes of atherosclerotic lesions and lesser numbers of macrophage

81 significantly upregulated on macrophages in atherosclerotic lesions and M1 macrophages in vitro.

82 oaded foam cell macrophages are prominent in atherosclerotic lesions and play complex roles in both i

83 Monocyte-derived macrophages, located in atherosclerotic lesions and presenting heterogeneous phe

84 rystal deposition that are characteristic of atherosclerotic lesions and pulmonary alveolar proteinos

85 sis factor-alpha, and interleukin-12) within atherosclerotic lesions and spleens of high-fat diet-fed

86 RT6 in the inflammatory pathways of diabetic atherosclerotic lesions and suggest its possible positiv

87 we observed that PIAS3 levels are reduced in atherosclerotic lesions and that PIAS3 expression decrea

88 Both the chronic development of atherosclerotic lesions and the acute changes in lesion

89 NZW rabbit aorta for detection of lipid-rich atherosclerotic lesions, and (2) on live animals for dem

90 s of inflammation including amyloid plaques, atherosclerotic lesions, and arthritic joints.

91 ion, the content of monocytes/macrophages of atherosclerotic lesions, and attenuated atheroprogressio

92 Atherosclerotic lesions are believed to grow via the rec

93 Advanced atherosclerotic lesions are further weakened by the pron

94 ioplasty for the treatment of infrapopliteal atherosclerotic lesions are not well characterized.

95 Surprisingly, however, mean atherosclerotic lesion area in Pggt1btriangle up/triangl

96 MAO levels in donors and recipients and with atherosclerotic lesion area in recipients.

97 A similar obese phenotype and increased atherosclerotic lesion area was displayed in LDL recepto

98 se inhibition blocked NET formation, reduced atherosclerotic lesion area, and delayed time to carotid

99 ecule MAP4K4 inhibitor also markedly reduces atherosclerotic lesion area.

100 unostaining was observed in the left carotid atherosclerotic lesions as a consequence of artery ligat

101 unity, which can be regulated locally within atherosclerotic lesions, as well as in secondary lymphoi

102 and CD163 receptors preferentially exist in atherosclerotic lesions at sites of intraplaque hemorrha

103 part, from decreased emigration of DCs from atherosclerotic lesions because of the high-cholesterol

104 PfnHet) exhibited a significant reduction in atherosclerotic lesion burden and vascular inflammation.

105 g (QKI) are low in monocytes and early human atherosclerotic lesions, but are abundant in macrophages

106 ge foam cells are characteristic features of atherosclerotic lesions, but the mechanisms linking chol

107 inical practice, in vivo characterization of atherosclerotic lesions causing myocardial infarction, i

108 ckout (DKO; apoE-CD16 DKO) mice have reduced atherosclerotic lesions compared with apoE knockout mice

109 lipidemic mice lacking ABCG1 develop smaller atherosclerotic lesions compared with controls.

110 ays an important role in the localization of atherosclerotic lesions concomitant with LOX-1 dependent

111 Advanced atherosclerotic lesions contain senescent cells, but the

112 osphorylated p53 compared with controls, and atherosclerotic lesions contained fewer proliferating ma

113 (99m)Tc-cAbVCAM1-5 uptake in atherosclerotic lesions correlated with the level of VCA

114 x, and immunohistochemical staining of human atherosclerotic lesions demonstrates similar staining pa

115 but not interferon gamma failed to increase atherosclerotic lesions despite partial reconstitution i

116 Atherosclerotic lesions develop in regions of disturbed

117 t macrophage phenotype and function and thus atherosclerotic lesion development and stability will he

118 Myeloid cells are central to atherosclerotic lesion development and vulnerable plaque

119 Intimal macrophage infiltration promotes atherosclerotic lesion development by facilitating the a

120 MitoOS in lesional macrophages amplifies atherosclerotic lesion development by promoting NF-kappa

121 oe deficiency) demonstrated no difference in atherosclerotic lesion development compared with apoe(-/

122 ry choline or TMAO significantly accelerates atherosclerotic lesion development in ApoE-deficient mic

123 ndogenous macrophage foam cell formation and atherosclerotic lesion development in apolipoprotein e(-

124 Moreover, perhexiline administration reduced atherosclerotic lesion development in apolipoprotein E-d

125 First, atherosclerotic lesion development in hyperlipidemic apo

126 poietic Fas deficiency does not affect early atherosclerotic lesion development in Ldlr(-/-) mice.

127 Atherosclerotic lesion development in response to high-c

128 these in vitro findings were of relevance to atherosclerotic lesion development in vivo.

129 on of various cell types that participate in atherosclerotic lesion development, including endothelia

130 ifferentiation of leukocytes is important in atherosclerotic lesion development.

131 flow in promoting atheroprone phenotypes and atherosclerotic lesion development.

132 Macrophages accumulate in atherosclerotic lesions during the inflammation that is

133 Stent System] for the Treatment of a De Novo Atherosclerotic Lesion [EVOLVE]; NCT01135225).

134 Intimal lymphatics in the atherosclerotic lesions exhibited an atypical phenotype,

135 Lipid-rich atherosclerotic lesions exhibited distinct positive TS (

136 essed a cleavage-resistant variant of MerTK, atherosclerotic lesions exhibited higher macrophage MerT

137 stochemical examination showed that VSMCs in atherosclerotic lesions expressed p16(INK4a), p14(ARF) a

138 f the crucial step in the mechanism by which atherosclerotic lesions form.

139 sing serum HSP27 levels both reduced de novo atherosclerotic lesion formation and enhanced features o

140 tes and macrophages promotes and accelerates atherosclerotic lesion formation by hyper-sensitizing mo

141 Whereas Cramp/DNA complexes aggravated atherosclerotic lesion formation in apolipoprotein E-def

142 versed vascular inflammation and accelerated atherosclerotic lesion formation in cholesterol-fed Ldlr

143 cruitment into the arterial wall and limited atherosclerotic lesion formation in hyperlipidemic mice.

144 =12-15) or SMCs (n=13-24) markedly increased atherosclerotic lesion formation in hyperlipidemic mice.

145 ompartment and was associated with increased atherosclerotic lesion formation in low-density lipoprot

146 R2 and its proresolving ligand annexin A1 to atherosclerotic lesion formation is largely undefined.

147 The rate of atherosclerotic lesion formation is profoundly influence

148 se to biochemical and biomechanical stimuli, atherosclerotic lesion formation occurs from the partici

149 found that FKN is expressed at all stages of atherosclerotic lesion formation, and that the number of

150 on of FPR2 or its ligand annexin A1 enhances atherosclerotic lesion formation, arterial myeloid cell

151 MPhi-IGF1R-KO significantly increased atherosclerotic lesion formation, as assessed by Oil Red

152 cy in atherosclerosis-prone mice accelerates atherosclerotic lesion formation, but the underlying mec

153 tial to provide a comprehensive insight into atherosclerotic lesion formation, diagnostics and respon

154 of Ldlr-/- Arhgef1-/- with WT BM exacerbated atherosclerotic lesion formation, supporting Arhgef1 act

155 responses are recognized as major drivers of atherosclerotic lesion formation.

156 nd then analyzed for plasma lipid levels and atherosclerotic lesion formation.

157 ncrease susceptibility to EC dysfunction and atherosclerotic lesion formation.

158 s and how these may mediate their effects in atherosclerotic lesion formation.

159 a-like 1 homolog (Dlk1) and thereby prevents atherosclerotic lesion formation.

160 nd fed an atherogenic diet showed aggravated atherosclerotic lesion formation.

161 monocyte chemotaxis in vivo, and accelerated atherosclerotic lesion formation.

162 Csn5 in Apoe(-/-) mice markedly exacerbated atherosclerotic lesion formation.

163 mice accelerated high-fat diet (HFD)-induced atherosclerotic lesion formation.

164 nd 46 quantification methods to characterize atherosclerotic lesions from (18)F-FDG PET images.

165 The presence of eRNA was revealed in atherosclerotic lesions from high-fat diet-fed low-densi

166 Peritoneal macrophages and atherosclerotic lesions from Zfp148(gt/+)Apoe(-/-) mice

167 Atherosclerotic lesions grow via the accumulation of leu

168 that influence both glucose homeostasis and atherosclerotic lesion growth.

169 Molecular imaging of atherosclerotic lesions has become a major experimental

170 Although extensively calcified atherosclerotic lesions have been proposed to be clinica

171 sible for the development and progression of atherosclerotic lesions have not been fully established.

172 These findings suggest that reduced atherosclerotic lesion in apoE-Fcgamma-chain DKO mice is

173 bin on the NLRP3 inflammasome inhibition and atherosclerotic lesion in ApoE2Ki mice fed a high-fat We

174 of cathepsin S attenuates the progression of atherosclerotic lesions in 5/6 nephrectomized mice, serv

175 rable uptake of [(18)F]FDM and [(18)F]FDG in atherosclerotic lesions in a rabbit model; [(18)F]FDM up

176 for 16 weeks developed significantly larger atherosclerotic lesions in aortic roots, aortic arches,

177 ize, stage, and inflammatory cell content of atherosclerotic lesions in Apoe(-/-) mice on high-fat di

178 miR-155 are selectively upregulated in early atherosclerotic lesions in Apoe(-/-) mice.

179 CIH caused more pronounced atherosclerotic lesions in ApoE-p50-DKO mice on a normal

180 nockout significantly reduced SPC numbers in atherosclerotic lesions in apolipoprotein E (ApoE)-defic

181 Unstable atherosclerotic lesions in carotid arteries require surg

182 Smad1/5 is highly activated in ECs of atherosclerotic lesions in diseased human coronary arter

183 fter dexamethasone treatment and in advanced atherosclerotic lesions in fat-fed Ldlr(-/-) mice.

184 NR4A1, TR3, or NGFI-B, is expressed in human atherosclerotic lesions in macrophages, endothelial cell

185 (SPIOs) and quantum dots was able to detect atherosclerotic lesions in mice after intravenous and in

186 erotic plaques in humans as well as advanced atherosclerotic lesions in mice demonstrated activation

187 type, and decreased the progression of early atherosclerotic lesions in mice.

188 orse use of insulin therapy for treatment of atherosclerotic lesions in patients with type 1 diabetes

189 interrogate the pharmacological response of atherosclerotic lesions in situ and in vivo.

190 ibited vascular inflammation, and suppressed atherosclerotic lesions in streptozotocin (STZ)-induced

191 acilitate the in vivo noninvasive imaging of atherosclerotic lesions in terms of intimal macrophage a

192 okines, alveolar bone loss, cholesterol, and atherosclerotic lesions in the aorta and aortic sinus co

193 okines, alveolar bone loss, cholesterol, and atherosclerotic lesions in the aorta and the heart compa

194 at high levels, and after 12 weeks, mice had atherosclerotic lesions in the aorta.

195 r heterozygous Tet2 knockout mice had larger atherosclerotic lesions in the aortic root and aorta tha

196 Atherosclerotic lesions in the aortic root, fasting plas

197 a cholesterol levels and three times smaller atherosclerotic lesions in the aortic roots.

198 ncy intravascular ultrasound (IVUS) revealed atherosclerotic lesions in the regions with augmented IS

199 5.64+/-1.89%; P<0.01 for both) and decreased atherosclerotic lesions in the subaortic sinus (158.1+/-

200 red with ApoE(-/-) mice, suggesting that the atherosclerotic lesions in these mice were not only larg

201 to VCAM-1 and allowed the ex vivo imaging of atherosclerotic lesions in Watanabe heritable hyperlipid

202 pendent reduction of LKB1 levels occurred in atherosclerotic lesions in western diet-fed Ldlr(-/-) an

203 rosclerosis and show that they accumulate in atherosclerotic lesions in which they directly affect pl

204 -/-)LKB1(fl/fl)LysM(cre) mice developed more atherosclerotic lesions in whole aorta and aortic root a

205 ubjects with FLI >/=60 are at higher risk of atherosclerotic lesions, independently of established ri

206 echanisms that underlie its pivotal roles in atherosclerotic lesion initiation and progression; explo

207 now widely accepted that the development of atherosclerotic lesions involves a chronic inflammatory

208 (s) that regulates T-cell trafficking to the atherosclerotic lesions is also unknown.

209 olipoprotein A1 (apoA1) recovered from human atherosclerotic lesions is highly oxidized.

210 ectly contributes to monocyte recruitment to atherosclerotic lesions is not known.

211 However, the mechanism of C3 accumulation in atherosclerotic lesions is not well elucidated.

212 The molecular basis for the focal nature of atherosclerotic lesions is poorly understood.

213 e (MPO) secreted by activated macrophages in atherosclerotic lesions is the promoter of such apoA-I o

214 the observed gain of DNA methylation in the atherosclerotic lesions justifies efforts to develop DNA

215 d that CaMKIIgamma-deficient macrophages and atherosclerotic lesions lacking myeloid CaMKIIgamma had

216 that Ogg1 expression decreases over time in atherosclerotic lesion macrophages of low-density lipopr

217 In the atherosclerotic lesion, macrophages ingest high levels o

218 TREM-1 was expressed in human atherosclerotic lesions, mainly in lipid-rich areas with

219 cid (LPA), a potent bioactive lipid found in atherosclerotic lesions, markedly induces smooth muscle

220 n of the antimicrobial peptide Cramp/LL37 in atherosclerotic lesions may thus stimulate a pDC-driven

221 DOL-induced dyslipidemia caused formation of atherosclerotic lesions of an intermediate stage, which

222 primarily by monocytes/macrophages in aortic atherosclerotic lesions of ApoE(-/-) mice and is secrete

223 Aortic arch atherosclerotic lesions of ApoE(-/-) mice were successfu

224 lood mononuclear cell (PBMC) accumulation in atherosclerotic lesions of cardiovascular (CV) patients

225 poptosis of insulin-resistant macrophages in atherosclerotic lesions of ob/ob.Ldlr(-/-) and Insr(-/-)

226 d T cells specific for CpPLD that infiltrate atherosclerotic lesions of patients with C. pneumoniae a

227 in activated T cells that infiltrate in vivo atherosclerotic lesions of primary APS patients with ath

228 d NKT cells were identified in the liver and atherosclerotic lesions of recipient mice.

229 arolimus-eluting stent implantation in focal atherosclerotic lesions of the internal pudendal arterie

230 Atherosclerotic lesions on aortic preparations were anal

231 ks, respectively, displayed similar areas of atherosclerotic lesions on cross sections of aortic root

232 determine whether their key roles are within atherosclerotic lesions or secondary lymphoid organs.

233 to describe the presence of T cells in mouse atherosclerotic lesions; other articles demonstrated the

234 P2X7 receptor was higher expressed in murine atherosclerotic lesions, particularly by lesional macrop

235 ed more trafficking of Ly6c(hi) monocytes to atherosclerotic lesions, preferential differentiation of

236 It has been known for some time that atherosclerotic lesions preferentially develop in areas

237 The earliest atherosclerotic lesions preferentially develop in arteri

238 a role in macrophage-driven inflammation in atherosclerotic lesions, probably by augmenting the Ccl5

239 Inhibition of IL-17A markedly prevented atherosclerotic lesion progression (p = 0.001) by reduci

240 that functional blockade of IL-17A prevents atherosclerotic lesion progression and induces plaque st

241 tibodies in autoimmune mice that targeted 25 atherosclerotic lesion proteins, including essential com

242 Identifying metabolically active atherosclerotic lesions remains an unmet clinical challe

243 cardiovascular disease have well-established atherosclerotic lesions, rendering lesion regression of

244 tween this optical index and the severity of atherosclerotic lesions, represented by the age of the r

245 ations suggest that macrophage activation in atherosclerotic lesions results from extrinsic, proinfla

246 In early atherosclerotic lesions, Rgs1 regulates macrophage accum

247 Analyses of atherosclerotic lesions showed that Acat1(-M/-M) reduced

248 sed glomerular filtration rate and increased atherosclerotic lesion size and aortic leukocyte numbers

249 ied novel QTLs that have major influences on atherosclerotic lesion size and glucose homeostasis.

250 HDCA supplementation significantly decreased atherosclerotic lesion size at the aortic root region, t

251 Atherosclerotic lesion size at the aortic root was simil

252 prisingly, the net effect was an increase in atherosclerotic lesion size due to an increase in the co

253 it did lead to a significant 60% increase in atherosclerotic lesion size in Pon3KO mice on the C57BL/

254 ne levels, blood pressure, oxidative stress, atherosclerotic lesion size in the aortic roots, cell pr

255 Atherosclerotic lesion size was decreased to levels obse

256 METHODS AND No difference in atherosclerotic lesion size was found in Ldlr(-/-) (low-

257 ct differences in fasting plasma glucose and atherosclerotic lesion size when deficient in apolipopro

258 umber of circulating blood monocytes impacts atherosclerotic lesion size, and in mouse models, elevat

259 suggestive QTL on Chr4, were identified for atherosclerotic lesion size.

260 ally, repeated treatment with Ac2-26 reduces atherosclerotic lesion sizes and lesional macrophage acc

261 In human atherosclerotic lesions, SMCs and ECs colocalized with I

262 , increased (18)F-FLT signal was observed in atherosclerotic lesions, spleen, and bone marrow (standa

263 the CORAL (Cardiovascular Outcomes in Renal Atherosclerotic Lesions) study, we performed exploratory

264 e observe increased P2X7 expression in human atherosclerotic lesions, suggesting that our findings in

265 The focal nature of atherosclerotic lesions suggests an important role of lo

266 Increased TLR7 expression in human atherosclerotic lesions suggests its involvement in athe

267 (Ldlr(-/-)), they develop larger aortic root atherosclerotic lesions than Ldlr(-/-) controls despite

268 rol diet, P2X7-deficient mice showed smaller atherosclerotic lesions than P2X7-competent mice (0.162

269 ormoglycemic ApoE(-/-) mice developed larger atherosclerotic lesions than sham-operated on controls.

270 marrow transplant developed 2.1-fold larger atherosclerotic lesions than wild-type bone marrow-trans

271 ase is often triggered by a distinct type of atherosclerotic lesion that displays features of impaire

272 ists even in phenotypically modulated SMC in atherosclerotic lesions that show no detectable expressi

273 hat are likely present in the vessel wall in atherosclerotic lesions, the effects promote atherogenes

274 Because of their rare detection in atherosclerotic lesions, the involvement of neutrophils

275 In atherosclerotic lesions, the miR-342-5p antagomir upregu

276 We have shown that in atherosclerotic lesions there is expression of MICA on e

277 eiden transgene that sensitizes the mice for atherosclerotic lesions through elevated plasma choleste

278 ein (LDL) is involved in the pathogenesis of atherosclerotic lesions through the formation of macroph

279 ile at rest and angiographically significant atherosclerotic lesions to angioplasty with a paclitaxel

280 f PTEN was observed in intimal SMCs of human atherosclerotic lesions underlying the potential clinica

281 th reduction in size and loss of lipids from atherosclerotic lesions upon plasma lipid lowering witho

282 ore, relative macrophage content in advanced atherosclerotic lesions was decreased.

283 frequent presence of T lymphocytes in human atherosclerotic lesions was first described in the 1980s

284 he endothelium, and accelerated formation of atherosclerotic lesions was observed in Senp2(+/-)/Ldlr(

285 Consequently, a marked reduction in atherosclerotic lesions was observed.

286 The influx of these cells into atherosclerotic lesions was significantly reduced, where

287 In murine atherosclerotic lesions, we found that macrophages turn

288 ly, structural and biochemical features from atherosclerotic lesions were acquired in ex vivo human c

289 thirty-two patients with 158 infrapopliteal atherosclerotic lesions were enrolled.

290 ipid levels and the extent and complexity of atherosclerotic lesions were examined and compared with

291 ecade ago, studies on macrophage behavior in atherosclerotic lesions were often limited to quantifica

292 as apoptosis and macrophage proliferation in atherosclerotic lesions were unaffected.

293 Moreover, L-sIDOL mice developed marked atherosclerotic lesions when fed a Western diet.

294 NCC is expressed in atherosclerotic lesions, where it colocalizes with IL18r

295 inantly expressed in foam cells found within atherosclerotic lesions, where MafB mediates the oxidize

296 ion or stroke, Apoe-/- mice developed larger atherosclerotic lesions with a more advanced morphology.

297 Treatment with GSO-494 results in smaller atherosclerotic lesions with increased plaque stability.

298 -derived fibroblast-like cells are common in atherosclerotic lesions, with EndMT-derived cells expres

299 ificantly reduced between early and advanced atherosclerotic lesions, with no loss in ABCA1 expressio

300 that is expressed in macrophages and within atherosclerotic lesions, yet its function in atheroscler